Chapter 7 Peripheral Nervous System (p.

248-256)
Somatic Nervous System:
1 neuron, a motor neuron, exits CNS and leads to target cells, skeletal muscle
fibers Neurotransmitter = acetylcholine (Ach)
o Nicotinic is the receptor type
Terminal button synapse = Neuromuscular Junction
o Where the skeletal muscle meets the somatic neuron
o Occurs in the motor end plate, this is only found on skeletal muscles
o Where the neuron meets and communicates with the skeletal muscle fibers
One neuromuscular junction on a skeletal muscle fiber
Somatic is only efferent enervation to skeletal muscle
Only depolarization elicited, so only cation channels opened EPP (end plate
potential)
A FIBER in a muscle means cell
Nicotine is the receptor in the skeletal muscle cell
Figure7.5:Eventsataneuromuscularjunction.
1.Anactionpotentialinamotorneuronispropagatedtotheaxonterminal(terminal
button).
2.ThislocalactionpotentialtriggerstheopeningofvoltagegatedCa2+channelsandthe
subsequententryofCa2+intotheterminalbutton.
3.Ca2+triggersthereleaseofacetylcholine(ACh)byexocytosisfromaportionofthe
vesicles.
4.AChdiffusesacrossthespaceseparatingthenerveandmusclecellsandbindswith
receptorchannelsspecificforitonthemotorendplateofthemusclecellmembrane.
5.Thisbindingbringsabouttheopeningofthesenonspecificcationchannels,leadingto
arelativelylargemovementofNa+intothemusclecellcomparedtoasmallermovement
ofK+outward.
6.Theresultisanendplatepotential.Localcurrentflowoccursbetweenthedepolarized
endplateandtheadjacentmembrane.
7.ThislocalcurrentflowopensvoltagegatedNa+channelsintheadjacentmembrane.
8.TheresultantNa+entryreducesthepotentialtothreshold,initiatinganaction
potential,whichispropagatedthroughoutthe
musclefiber.
9.AChissubsequentlydestroyedbyacetylcholinesterase,anenzymelocatedonthe
motorendplatemembrane,terminatingthemusclecellsresponse.

Any communication is excitatory so if you do not want to communicate

with a muscle or let it relax you just dont talk to it.
Skeletal muscle is Neurogenic the neuron tells the muscle to
contract, generates contraction of fiber
Neuromuscular Junction:
Somaticmotorneuronterminalbutton
Musclefiber(cell)
Motorendplateonlyfoundinskeletalmuscles,thisiswhereallthe
neuromuscularjunctionhappens
Acetylcholine(ACh)gatedcationchannels(increaseNa+andminorK+
permeability)
Containsvoltagegatedsodiumandpotassiumchannels
EndPlatePotential(EPP)

Acetylcholinesterase(AChE)theameansthereisanexnzyme,itbreaksdown
aCh.Killsoffneurotransmitter,weneedtokeepthatareaclean
InskeletalmuscletheNMJisinthemiddleofthefiber
Withthisweareonlygoingtoexciteourskeletalmusclefibers
ThisisonlygoingtobeexcitatoryNOinhibition
Skeletalmusclewillalwaysgettothresholdifthesomaticneuronfiresnomatter
what.Ifwillnotreachthresholdifsomethingdramaticallygoeswrongbutmost
ofthetime,always,itwillreachthresholdandfire.
Eachskeletalmusclefiberhasaneuromuscularjunction
Eachskeletalmusclefiberhastobetoldtocontract.
Eachindividualaxonterminalisconnectedtoaneuromuscularjunction

Selected Neuromuscular Agents

Black Widow Spider Venom
o Affects the NMJ by causing a burst of aCh in the button
o By this its flooding the synapse and the Acetylcholinesterase(AChE)can
not clean it up fast enough, this causes a massive contraction
o Not big a deal to us but to small things like mice it will be a problem
o Causes huge muscle contractions
Clostridium botulinum toxin (botulism, BoTox)
o Smallest amount to cause death, most lethal
o Bacteria that causes botulism
Ex. machine that labeled the salmon cans
o Its in botox
o It blocks the release of Ach so sarcoplasmic reticulum wont contract
o In very small doses they can get the small muscles to stop twitching
Curare
o Plant based drug from Africa
o Blocks the aCh cation channels
o Use to be used in surgeries to calm the muscles down
Organophosphates
o Not natural, military nerve gases
o Not organic so when it binds it binds permanently to Acetylcholinesterase
(AChE).Cantcleanoutthesynapsewhichcausestomassiveskeletal
contraction
o BandintheUS
o Permanentbinding
Myasthenia gravis (Neostigmine)
o A autoimmune disorder own immune system tags then attacks one of
your products
o The receptor-gated channel thinks its being bound or triggered by Ach so
it opens the cation channel.

o Down regulated Ach receptors, skeletal muscles become least sensitive to

Ach
o Starts in the face, start loosing facial expression. Problems with
swallowing can go down diaphragm.
o Neostigmine is the best drug for this. It binds to the Acetylcholinesterase
(AChE),thisdoesntallowthesynapsetobecleanedandbuildsupAch
soitcanbindtothesmallamountofAchreceptorsthatareleft.
Basic Structure of overall skeletal muscle:
Strong and flexible
Muscle FasicleMuscle Fiber cell (a single muscle cell)Myofibril (with
sarcomeres, functional unit)
Connective tissue around each fascicle, they are an insulator to get muscle fiber
fired, but it wont affect the fiber next to it.
Dark and light bands are the striations of the muscle
Sarcomere means flesh, functional unit
Muscle Fiber = Muscle Cell
Sarcolemma (covers the whole muscle cell), sarcoplasm (covers each individual
myofirbril)
Huge multinucleated cells
Transverse Tubules
Allow depolarization of the membrane to quickly penetrate to the interior
of the cell
Inside the sarcolemma
Sarcoplasmic Reticulum (lateral sacs)
Are surrounding the transvers tubules and then covers like a net all over
the muscle fibers
Surrounding the sarcomeres of the myofibrils

DRAW SARCOMERE FOR EXAM

Sliding Filament Theory
Thin filaments (of actin with troponin & tropomyosin) make-up the walls of
the sarcomere compartments
H zone is the lighter portion in the center of the A band where there are no
thin filaments
Calcium binds to troponin making tropomyosin move away and thick
filament will bind to the thin filament
Thick filaments (of myosin) make-up the central core, that pulls in the walls
A band is darker because of the presence of the thick filaments
The thick filament grabs the thin filament and pulls it towards the M-line
and shortens (CONTRACTION)
I-Band shrinks and H-zone shrink when sarcomere shorten, sarcomere shortens
and A-band remains the same length
FILAMENTS DO NOT CHANGE LENGTH they just overlap each other to
shorten the sarcomere
There are two binding sites
o Actin & ATP
o But you cannot bind to both at the same time
Cross bridge Cycle (connection between the thin and thick filaments)
Starting point = relaxed no contraction
Tropomysoin are blocking the binding sites
Myosin are cocked and ready which means ATP has been there and broken down
Acting kicks off only ADP = triggers power stroke
Then gets stuck and ATP binds to myosin head and releases
Cross bridge Cycling
Contraction
o When nervous system tells the muscle fiber to contract all the myofibrils,
sarcomeres contract
Troponin-tropomyosin complex
o At rest blocks myosin from grabbing actin - when contracting are moved with Ca2+
Cross bridges
o Myosin bound to actin (forms a bridge/connect)
Attach - power stroke - release - recock
1. Think Filament and myosin

2.
3.
4.
5.
6.

a. Muscle relaxed - myosin-head cocked & ready, just needs a binding site,
still bound to ADP
ATACHES: Myosin head binds when actin binding site becomes available (Ca2+
binds to troponin, moving tropomyosin out of the way) - knocking off ADP
POWERSTROKE: Myosin-head power strokes, pulling actin walls toward the
M-line
Releases: Myosin-head releases when ATP binds to it , If no ATP available
youre stuck: rigor mortis
Re-cocks: Myosin-head hydrolyzes (breaks) ATP to ADP and uses the energy to
recock the myosin-head. If Ca2+ still available then crossbridge cycle starts again.
a. Attach - Power stroke - Release - Recock
If Ca2+ no longer available - then the muscle has been returned to its cocked and
ready position
a. Muscle twitch = the smallest muscle contraction, in skeletal muscle
If Calcium is cleared out that doesnt mean they all stop at the same time, its like
pouring water out of a bucket. Some water touches the floor first then the rest
follows
Energy released is used to cock the myosin head
To get each myosin to release you need an ATP for each head
How are we using ATP?
o We use ATP to stop contraction by releasing it
o Heat can be given off as ATP

Cross Bridge Activity

1. Binding: Myosin cross bridge binds to actin molecule.
2. Power stroke: Cross bridge bends, pulling thin myofilament inward.
3. Detachment: Cross bridge detaches at end of power stroke and returns to original
conformation.
4. Binding: Cross bridge binds to more distal actin molecule; cycle repeats.
Excitation contraction coupling
Excitation is how do you generate the excitation in your skeletal muscle
o In the NMJ
o Excite sarcoplasmic reticulum drops its calcium and begins to suck it
back up again
o Always guaranteed to reach threshold unless something bad happens
o Somatic Nervous System
The contraction is the cross bridge cycle
o Pulling the thin filament to the m-line
BASICALLY going from NMJ to Cross Bridge Cycle
The trigger point is the voltage gated channels from the sarcoplasmic
reticulum is the intermediate point that brings the NMJ and the Cross bridge
cycle together
STEPS:

1. An action potential arriving at a terminal button of the neuromuscular junction

stimulates release of acetylcholine, which diffuses across the cleft and triggers anaction
potential in the muscle fiber.
2. The action potential moves across the surface membrane and into the muscle fibers
interior through the T tubules. An action potential in the T tubule triggers release of Ca2+
from the sarcoplasmic reticulum into the cytosol.
3) Ca2+ binds to troponin on thin filaments.
4) Ca2+ binding to troponin causes tropomyosin to change shape, physically moving it
away from its blocking position; this uncovers the binding sites on actin for the myosin
cross bridges.
5) Myosin cross bridges attach to actin at the exposed binding sites.
6) The binding triggers the cross bridge to bend, pulling the thin filament over the thick
filament toward the center of the sarcomere. This powerstroke is powered by energy
provided by ATP.
7) After the power stroke, the cross bridge detaches from actin. If Ca2+ is still present,
the cycle returns to step 5.
8) When action potentials stop, Ca2+ is taken up by the sarcoplasmic reticulum. With no
Ca2+ on troponin, tropomyosin moves back to its original position, blocking myosin
cross bridge binding sites on actin. Contraction stops and the thin filaments passively
slide back to their original relaxed positions.
3 ways we controlling strength on Contraction:
1. Twitch summation Calcium is going to control the strength, by controlling
calcium you control contraction, controlling each individual fiber
a. Larger and larger contractions as we sum the twitches
2. Length-tension relationship how much the muscle can stretch to how much the
muscle can contract
3. Motor unit / recruitment we only triggers a few fibers, not the whole muscle.
This is good to pick up a little object. When you pick up something heavy you
recruit more muscle fibers
Muscle fatigue: The inability to perform the action you are trying to do
o The Two things that cause muscle fatigue
a. Lack of ATP
b. Change in pH especially acidity lower pH, more alkaline will also make
an impact but less likely it will occur
Fig 8-13 Graph (TWITCH SUMMATION)

Skeletal Muscle Resting Membrane potential is about -90MV

o Means that it is potassiums equilibrium
o Very leaky to potassium
o When opening a cation channel Na going in because potassium is gone
from the membrane being very leaky to K
Skeletal muscle is about 1-2ms long just like nerve cell
The strongest part of the curve is in the middle where you have more calcium, that
means the most myosin heads are moving
The length of twitch varies 50-100ms length of twitch
Tetnus (tetanic) FULL FORCE TWITCH SUMMATION
o Biggest muscle contraction that a muscle can give you
o Can cause locked jaw
o Starts from the head
o High frequency/action potentials

Length-Tension Relationship
There is an optimal stretch in your muscle to give you max strength
As you over stretch you loose strength, you pull all myosin away from actin , they
actually cant reach they are just standing there staring
You want optimal overlap between the thick and the thin filaments
For ice skaters, they use their gluteus Maximus and lean forward/over to get their
optimal maximal strength stretch because it works best like this
Put muscle in the right place to get the max strength stretch
Found in skeletal muscle, smooth muscle doesnt have any its good because we
want to move fecal material down intestines. You do in cardiac muscle!
Difference is that in cardiac muscle:
The more you stretch the harder it contracts, the more blood you have in the heart
the heart will push it out faster and stronger, the more you stretch the heart the
stronger it contracts (natural length and tension relationship). If you receive 70ml
in heart you better pump out 70ml
Motor Unit
Is the somatic neuron plus all the fibers it connects to, For example: motor units
of 12 is 1 for somatic neurons and 11 fibers its communicating with.
Smallest are about 4
Fine control you want about 3 fibers, knitting
30,40,50 motor units are in your thighs
Come in different sizes
Allow us to activate a subset in the whole muscle
Somatic neurons only talk to the fibers
Benefits: ability to recruit, allows for a range of strengths from a given muscle,
very efficient with ATP use, avoiding fatigue, dont have to use the whole muscle

at once, it allows you to rotate through the motor units in the muscle to allow you
to use the muscle for a longer period of time
Its a learned process, for example sometimes you may recruit too many and the
object you are picking up is actually light, and sometimes you recruit less and the
object is very heavy
2year olds are still trying to learn the motor unit recruitment process
Rotate through the motor units, rotate through fibers by recruiting different
subsets of the muscles to allow the muscle to continue to work longer

Tension vs. Load

If picking up 20lbs you need to put 20lbs of tension
Load and strength and tension of muscle are directly related
GENERAL CONTRACTION TYPES
Essentric conrtraction controlling drop, elongating of muscle
Consentric contraction shortening of muscle
Isometric muscle length does not change
Fueling muscles (creatine phosphate)
Store it
Longer life then atp, but cant use it directly. it acts like a immediate
recharger for ADP
Recharge your old atp
Replenish atp with creatine phosphate if atp is available
Its in short supply, so go to cellular respiration for atp
replenish with respiration
charged with hi energy phosphate group
can store it
o Glycolytic (anaerobic) specialists
o Oxidative (aerobic) specialists
Glycolytic
Specialized for anaerobic respiration
2 ATP/glucose, but very rapid bursts of ATP production
lactic acid biproduct
fast but inefficient
White meat. Not that much myoglobin
Chickens
Bicep muscle
Usain Bolt
Oxidative
Specialized for aerobic respiration
~36ATP/glucose via high density of mitochondria
Myoglobin the protein ( has a higher O2 affinity than hemoglobin), this is
what makes dark meat dark

Highly vascular
efficient but slow
great for endurance, not huge burts
no lactic acid, byproducts are CO2 and H2O
great blood supply
Dark meat
o Example:
Erector spinae muscle
Mev

Different people have different proportion of glycolytic and oxidative

Genetics and environment have a lot to do with it
Skeletal Muscle Fiber Type (3)
Slow Oxidative (red, myoglobin) Type I
o Best at avoiding fatigue
o Not using atp as quickly
o Lots of atp and no lactic acid build up
o Cant change the slow to fast oxidative or fast glycolytic
Fast Oxidative (red, myoglobin) Type IIa
Fast Glycolytic (white) Type IIx
o Fatigue fast
o Biceps and shoulder muscles
o Few mitochondria
o High levels of glycogen
All muscles have all three fiber types - they vary with regard to specific muscle,
genetics, & training
You can change the proportions/ shifts from fast oxidative/glycolytic
Fiber size = fiber strength
ALL skeletal muscles in the body have all e of these muscles, different muscle
will have different proprtions of each type
Muscle Size:
Hypertrophy tissue or organ gets larger because cells inside get larger/bigger
not because cell number gets larger (thats hyperplasia)
o Adult liver is larger then child liver due to hyperplasia
o Skeletal muscle grows through hypertrophy
Atrophy: loss of muscle size, due to cells getting smaller
o 2 types:
o Disuse Atrophy
Not using it
Astronauts, arm out of cast
PT can decrease this
o Denervation Atrophy
Somatic neurons not firing to the fibers

 Muscle not receiving somatic nerve

o Muscular dystrophy
Loss of muscle tissue as a result of a lack of a protein called
dystrophin protein (in the sarcolemma it helps to maintain the
stability of that structure of that cell)
Individuals can be born without the protein or have a loss of this
protein as they grow older
We are loosing cells not size
It means any disease in which you get loss of muscle tissue
(degenerations), a much broader term than defined
Include the diaphragm/muscles of swallowing
Individuals who are not making enough or not making enough of
the protein and leads to destabilized sarcolemmas/cells begin to
die
Afferent Information back to brain
Nociceptors all skeletal muscles have this and proprioceptors
Proprioceptors
o Two types:
o Muscle Spindles (Knee-Jerk reflex)
Buried in muscle cell
collection of specialized intrafusal fibers that lie within a
connective tissue capsule parallel to the ordinary extrafusal skeletal
muscle fibers. Interverted by its own gamma motor neuron and is
supplied by two types of afferent sensory terminals, the primary
(annulospiral) endings and the secondary (flower-spray) endings,
both of which are activated by stretch.
o Golgi Tendons Organs
Buried in tendons
Entwined with the collagen fibers in a tendon and monitors
changes in muscle tension transmitted to the tendon.
Smooth & Cardiac&Skeletal Muscle
Skeletal

Smooth

Cardiac

Striated ( are from thick and thin

filaments, striations mean
sarcomeres)
Voluntary ( only contracts because
somatic NS tells it to, all control is
in the NS)
Fiber size is huge
Multinucleated (50-100)
Transverse tubules
Huge SR
Cocking of myosin head is
automatic
Somatic
Nociceptors/proproceptors

Un-Striated (no
sarcomeres), has thin
and thick filaments but
spread out like net, this
means no troponin
tropomysosin
components so Ca cant
bind.
Involuntary (affect by
hormones, irritation,
stretch, heat, controlled
by whole environment)
Fiber size is small
1 nucleus (fattest part of
cell)
Non existent (transverse
tubules)
Diffusion
Binding sites always
open
Cant cock own myosin
heads but calcium is the
trigger
Autonomic
If stretch, contracts back
myogenic

Striated (sarcomeres functions like

SM) striations mean sarcomeres
Involuntary (affect by hormones,
irritation, stretch, heat, controlled by
whole environment)
Fiber size is intermediate
1-2 nuclei
Not so much transverse tubules
Diffusion/SR uses both
Autonomic
If stretches it doesnt contract back
myogenic

Smooth Muscle
Spindle shaped
Dense bodies instead of sarcomeres they have this
Very slow myosin activity for energy conservation
Ca2+-Calmodulin 2nd Messenger System phosphorylated Myosin-head
activation LEADS TO THE COCKING OF THE MYOSIN HEADS
Very few signals that lead to a cascade of millions of reactions
Binding sits always available
ALL WE NEED TO KNOW IS THAT IT LEADS TO THE
COCKING OF THE MYOSIN HEADS
Tone, latch phenomenon
Always a little calcium in there which means that we always got cell
myosin heads going through their cycle, never really relaxed
Can control the tube size/tone of tube
Multiunit vs Single Unit Smooth Muscle
Mainly talk about single unit
Multi units (NEUROGENIC)smooth muscle means that the individual smooth
muscle cells act like individual units you have to talk to each cell independently.

Found in eye (to help focus), in the iris to help control dilation , attached to hair
follicles
Single units (MYOGENIC)smooth muscle, all the cells are inner connected by
huge numbers of gap junctions, like a tunnel that connects from one cell and the
next, a wave of activity, you just communicate with a small bundle of cells and
that will spread out. With that wave you have thousands of cells acting like one
unit. Functional syncytium. Found in all the tubing in body
Two Types of Smooth Muscle (these refer to what is going to cause the muscle
cell to contract, How do we excitation to skeletal muscle?)
o Neurogenic the nervous system telling muscle to contract
Multiunit smooth muscle
Affected by local environment (stretch, hormones, irritation)
o Myogenic muscle itself creates own excitement/contraction
Single units smooth muscle
Functional Syncytium
o In all organs to help move stuff across our bodies.
o Two Types of Smooth Muscle (functional syncytium)
o Ventricular fibrillation
When your cells come out of sync and the heart is not working as
one unit so they have to shock your heart with the electrodes to get
it to all function at the same time. You lost your functional
Syncytium.

Cardiac Muscle
Intercalated disc one cardiac muscle cell attaches to the next cardiac muscle
cell
o Desmosomes (strong but stretchy) and gap junctions in intercalated discs
o 1-2 nuceli
o myogenic (and in smooth muscle), cell has to create excitement
Single units muscles use these two , Auto rhythmicity: Slow-Wave vs. Pacemaker
Slow-Wave Potentials some single unit cells use this to alternate their ion
Single unit
permeability channels
cells use
both,
o Some Single-unit Smooth muscles
cardiac only
o Alternating ion permeabilitys - may or may not reach threshold
uses
pacemaker
o Cells have alternating channels creating wave of polarity
Pacemaker Potentials
o Cardiac & some Single-unit Smooth muscles
o Leaky to Na+ to threshold, at 60mv then you leak your way to threshold
o Involuntary, under control of the ANS
o Nervous system adjusts ion permeabilitys

These two can

affect how fast
or how slow
they will get to
threshold but
they dont run

o Under sympathetic innervation you release EPI and NOREPI,

they make the cells leakier, leaks it faster and this causes it the
increase rhythm of heart
o Under Para releases Ach and makes you less leaky, closes up
channels, takes longer to leak your way to threshold and makes
heart rhythm slower

Cardiovascular system
o Artery, Arteriole, Capillary (only sight for exchange between blood and tissue,
pick up waste products like CO2), Venuole, Vein
Systemic circulation the right side of the heart sends deoxygenated blood to the lungs
to get refreshed, to get oxygenated. The left side of the heart receives oxygenated blood
from pulmonary circulation and pumps it to the systemic circulation (rest of body)
In lungs fragile, low blood pressure, the volumes in the lungs are the same, pumping at
the same time. Time and volume are the same for right and left lung, its the pressures
that are completely different. Giraffe has the greatest blood pressure difference because
of how separated his head is from the rest of the body.
Tracing a blood cell through the heart!
Inferior/Superior Vena CavaRight Atrium Right Atrioventricular ValueRight
Ventricle Pulmonary Semilunar Valve Pulmonary Artery Lungs Pulmonary
Veins Left Atrium Left Atrioventricular Valve Left Ventricle Aortic Semilunar
Valve Aorta Systemic Circulation
Beats of the heart
o 1st beat slamming shut of the Atroventricular Valves
o 2nd beat Semilunar Valves Shut down
o Its also good to know that the ventricles work harder if the pressure on the other
side of the valve is greater.
o You also get the same blood pressure from the leg and arm

- Use pacemaker potentials to get beats

- Ventricles contract bottom to top
- If there are no blood in ventricles they will collapse, no air or open space
- Right and Left sides eject same amount of heart, if not you will get a back up in the system
-Arteries are elastic
-Heart beats 70bpm

Valves:
One way valves
Laminar Flow do not hear it, its when you get turbulence, its always smooth,
this is how blood should always flow
What holds down the ventricles so blood wont go backwards?
Pupillary muscle, the cords are called chordae tendineae
You also never eject all the blood, only about 50%
4 major pacemaker cluster cells: (this is under parasympathetic stimulation, at rest)
1. Sinoatrial Node
a. This is our fastest node, it leaks to threshold the fastest
2. Atrioventricular Node
a. Sending signals to the ventricles
3. Bundles of his with bundle branches
a. Sending signals to the ventricles
4. Purkinjie fibers
a. Communicating with actual muscles
*All these cells are capable of leaking themselves to threshold
Plateau phase
Open voltage gated calcium channels, calcium goes in K goes out. Theyre
charges are canceling each other out.

Electrocardiogram measures change in electricity in your body

Heart is creating the electrical system
We dont see the atria repolarization because thats when the ventricles depolarize
Ventricles are the most full right before they eject
Cardiac function
Systole (between P and QRS)
o Contraction
Diastole
o Relaxation
Stroke volume (SV) = end diastolic volume end systolic volume
o Ejection volume, how much volume of blood do the ventricles contract
EDV Ventricles are most full
o Volume at the End of ventricle relaxtion phase
ESV Ventricles are least full
o Volume After ventricles contract
Isovolumetric contraction (all valves are shut)
All four valves shut
Between QRS and T
Pop open semilunar valve
Isovolumetric relaxation (all valves are shut)
Pop up open AV
After the C
T or F during atrial contractions the semilunar valves are open
Dicrotic Notch blood bouncing valves when they close shut. Blood causing
little waves

Repolarization is the return of the ions to their previous resting state,

which corresponds with relaxation of the myocardial muscle
electrical impulse causes the ions to cross the cell membrane and causes
the action potential, also called depolarization

Cardiac Disorders
Arrhythmias Iregular Heart Beat
Bradycardia slow resting HR, HR<50, only exception are athletes
Tachycardia Fast resting HR, HR>100
Premature ventricular contraction Ventricles cause an extra beat
Complete heart block Scar Tissue, The atria is beating faster than
ventricles
Ectopic focus irritation or inflammation
Atrial or Ventricular Fibrillation For atria fibrillation you are not
ejecting blood anywhere, get defibrillator. Not getting a functional
syncytium meaning that the gap junctions are not running the show
o Loose all pumping contraction

o No Ventricular fibrillation medicine

Heart Sounds
Lub & dup
Heart murmurs abnormal heart sound, caused by valve problems
Stenotic valves The valves are stiff and do not open up all the way,
causes turbulence. Makes whisper noise
Insufficient valves, regurgitation
Not closing right, you are getting regurgitation of blood
backwards. Bubbling noise
Laminar vs. turbulent flow
When you get turbulent you can hear it
Cardiac output
How hard the heart is beating
At rest pumping about 5L of blood
Cardiac Output (CO) = stroke volume x heart rate
Cardiac reserve = COmax COrest
Frank-Starling Law
DEF> The cardiac muscle fibers length, which is determined by the extent of
venous filling, is normally less than the optimal length for developing maximal
tension. Therefore, an increase in end-diastolic volume (that is, an increase in venous
return), by moving the cardiac muscle fiber length closer to optimal length,
increases the contractile tension of the fibers on the next systole. A stronger
contraction squeezes out more blood. Thus, as more blood is returned to the heart
and the end-diastolic volume increases, the heart automatically pumps out a
correspondingly larger stroke volume.
Cardiac muscle length-tension relationship
End-diastolic volume stretches heart
Heart failure SV decreases at the same EDV as normal heart
During compensation for heart failure, reflex sympathetic stimulation
shifts the FrankStarling curve of a failing heart to the left, increasing the
contractility of the heart toward normal. A compensatory increase in enddiastolic volume as a result of blood volume expansion further increases
the strength of contraction of the failing heart. Operating at a longer
cardiac muscle fiber length, a compensated failing heart is able to eject a
normal stroke volume
Congestive heart failure
Cardiac Blood Flow
Myocardial ischemia
o Blood flow to your heart muscle is decreased by a partial or complete
blockage of your heart's arteries (coronary arteries). The decrease in blood
flow reduces your heart's oxygen supply.

Myocardial infarction (heart attack)

Coronary artery disease (CAD)
Atherosclerosis
Thrombus
Embolus
Occlusion
o Loss of blood flow in a region of the heart
o When vessels contract it squeezes heart
o Metabolic activity really active tissue= increase blood flow
The higher the activity the higher vasodilation of coronary vessels
Chapter 10 Blood Vessels
Arteries Arterioles Capillaries Venioles Veins
Away from
heart
(elastic
wall)

Only place of
exchange
between
blood &
tissues

Returning
blood to
heart

Arteries
Away from the heart
Thick, elastic walls
High pressure
Arterioles
Control to the tissues
Walls mostly smooth muscle
Constricting walls decreases blood flow
Capillaries
Only site of exchange (between tissues & bloood)
Only one squamous cell thick (endothelial cell)
Venules
Very tiny veins
Veins
Very loose, baggy walls
Contricting walls increases blood flow (venous return)
Very low pressure, returns blood to the heart

*If you have all the blood vessels open your blood pressure drops significantly
*Most coronary blood flow occurs during diastole because the coronary vessels are
compressed almost completely closed during systole.
Blood Vessel Diameter
Vascular tone
Vasoconstriction
Vasodilation

active hyperemia (fig. 10-10, p 353)

Local vasoactive mediators (NO, endothelin; histamine)
Other factors: temperature, sympathetic nervous system

Capillary Exchange
Capillary beds
Precapillary sphincter
Pores
List and Define the ways exchange across a capillary occur
Diffusion small molecules that can move high concentration to
low concentration (Na and Cl leaving) through channels or
through the cell
Transcytosis move larger things through capillary walls by
exocytosis and endocytosis. The way you move larger molecules
like insulin
Bulk Flow Bulk flow is the result of filtration and reabsorption
between the capillaries and the interstitial fluid due to fluxes in
blood pressure and osmotic pressures
Bulk flow
Filtration pushing fluids put through capillary wall
Reabsorption forcing fluids out and sucking them in. The way you clean/rinse
tissues
The more you increase BP the increase the filtration and the less absorption
happens
Anything that increases filtration or reabsorption gets the extra fluid in the tissues.
This causes EDEMA
o Edema can be localized or systemic
o Edema as a result of increases in capillary blood pressure, capillary
permeability, interstitial fluid colloid osmotic pressure (inflammation)
o Filtration is a constant process, its high in the beginning and decreases in
the end
Blood Flow in the Veins
Venous capacity, venous return
Venoconstriction (vasoconstriction of veins) improves flow
Skeletal muscle pump, respiratory pump, heart as suction pump and force of
blood pressure
Many veins have valves, constricted skeletal muscles act as transient valves
Blood volume at rest is usually in the systemic veins
Vasopressin
Constrict blood vessel, increases BP
Another word for this is ADH, anti diuretic hormone

Blood volume increase with ADH and helps BP

Found in posterior pituitary

Medullary CV control center & hormones

Afferent:
Carotid sinus & aortic arch baroreceptors
Cardiovascular Control Center in medulla oblongata of brain stem
Efferent: (bodys emergenry to increase BP)
Autonomic N.S.
Vasopressin
Renin-angiotensin-aldosterone system, increase MAP
Disorders
Coronary artery disease (CAD) this is atherosclerosis of the heart
Atherosclerosis plaque usually forms an eclusion = inflamation
Thrombus problem for blood flow but trouble Is when it breaks free then
becomes an embolus which turn into thromb, blood clot or plaque
Embolus anything blocking a vessel
Occlusion cant get into any artery
Hypotension systolic under 100mmhg, low blood pressure
Hypertension high blood pressure
Circulatory shock sudden drop in BP
Hemorrhage Bleeding
Circulatory Shock (decreases MAP)

Hypvolumetric shock (decreases CO)

o

Severe blood and fluid loss

o Less BV
o BP decreases
o Pass out to save the brain because the blood gets to the brain faster when
you are horizontal
o Uses anaerobic respiration
o Lactic acid build up, keep them warmer

Cardiogenic shock(decreases CO)

o Heart is problem, weakened heart, result of long term age and disease
o Heart not able to get proper SV, BP decreases
Vasogenic shock(Decrease TPR)
o Problem with blood vessel
o Infection or allergic reaction can be the cause
Ex. sting ray example
o Massive Vasodilation so there will be a TPR decreases
o Septic shock and anaphalactic shock

Neurogenic shock (Decrease TPR)

o Problem with ANS
o Lost of vascular tone
o Decreases Sympathetic system: increases
contractility
Increases venous return
And increase HR

These are also 3

ways to
increase Stroke
Volume

3 ways the Cardiac Output is affected?

1. Increase HR by increase SA node
2. Increase contracting of muscle
3. Increase tone or vasoconstriction of veins, which increases
venous return